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Elevated tumor necrosis factor-alpha in skeletal muscle after stroke
Charlene E Hafer-Macko1, Shuzhen Yu, Alice S Ryan
1Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. cmacko@grecc.umaryland.edu
Stroke
|August 20, 2005
Summary
Tumor necrosis factor-alpha (TNF-alpha) mRNA levels are elevated in the paretic leg muscles of stroke patients, indicating accelerated inflammatory pathways. This suggests a potential role for TNF-alpha in stroke-related muscle atrophy and metabolic issues.
Area of Science:
- Neuroscience
- Immunology
- Metabolism
Background:
- Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine linked to muscle wasting and insulin resistance.
- Stroke is associated with muscle atrophy, diabetes, and insulin resistance.
- TNF-alpha expression in hemiparetic skeletal muscle has not been previously studied.
Purpose of the Study:
- To investigate elevated TNF-alpha mRNA levels in the paretic leg muscles of chronic ischemic stroke patients compared to non-paretic legs and healthy controls.
- To explore the role of inflammation in stroke-induced muscle changes.
Main Methods:
- Muscle biopsies were obtained from the vastus lateralis of 20 stroke patients and 9 controls.
- Total RNA was extracted, reverse transcribed to cDNA, and TNF-alpha transcripts were quantified using real-time quantitative polymerase chain reaction.
- TNF-alpha mRNA levels were normalized against a housekeeping gene (acidic ribosomal phosphoprotein).
Main Results:
- TNF-alpha mRNA levels were 2.8-fold higher in the paretic leg muscles of stroke patients compared to controls (P<0.03).
- Non-paretic leg muscles showed a 1.6-fold increase in TNF-alpha mRNA compared to controls (P<0.11).
- A trend towards higher TNF-alpha mRNA levels was observed in paretic versus non-paretic leg muscles.
Conclusions:
- Stroke patients exhibit increased TNF-alpha expression in their paretic leg muscles.
- These findings suggest that inflammatory pathways are activated in the skeletal muscle following stroke.
- Further research is warranted to determine if intramuscular TNF-alpha contributes to muscle atrophy and metabolic dysfunction post-stroke.